Detection and stabilization or reduction of vulnerable plaque motivates the current research in vulnerable plaque diagnosis and treatment. The rupture of unstable or vulnerable atherosclerotic plaques located on the walls of coronary arteries, the carotid arteries, and other cardiovascular arteries, combined with associated thrombosis, is recognized as a common cause of acute coronary syndrome (ACS) such as unstable angina, myocardial infarction, and sudden ischemic cardiac death.
Vulnerable plaque is often formed in the vessels of the heart, vessels supplying blood to the brain, and other cardiovascular arteries. It largely goes undetected, though its shape and composition make it susceptible to disruption, resulting in blood clots that can cut the supply of blood to the heart or brain, producing chest pain, heart attack or stroke.
Vulnerable plaques are small lesions typically comprising a lipid-rich core, surrounded by a thin, collagenous cap with varying degrees of smooth muscle cells. The vulnerable plaques form within the walls of cardiovascular vessels, and are often eccentric in shape with irregular borders. The plaques may be characterized by a thickened arterial wall, partial stenosis, and generally elliptical distortion of the cardiovascular lumen with blockages ranging from zero up to about 70%. Stenoses are generally less severe with vulnerable plaques than stable plaques. However, mild stenoses are far more common and are responsible for more occlusions than tighter stenoses. Vulnerable plaques may be differentiated by their size, shape and composition of their lipid cores and fibrous caps. Acute lesions are larger with crescent-shaped cores rich in cholesterol esters with extracellular lipid accumulation. The fibrous cap may be infiltrated with macrophages throughout and at the borders in contact with normal intima, a precursor to initiating the disruption of the vulnerable plaque with mechanical strain or degradation of the wall thickness.
The fibrous cap may fatigue and rupture from mechanical stresses, releasing macrophages and tissue factor leading to thrombosis. Tension within the cap occurs with elevated blood pressure and larger vessel radius. Cyclical tension and compression of the cap occurs with normal systolic-diastolic pressure changes that increases with faster heart rate and increased activity. Bodily movements and physical exertion may stress the plaque and exacerbate the onset of fissures in the cap. The cap may also degrade from the secretion of proteolytic enzymes such as plasminogen activators and metalloproteinases from lipid-filled macrophages (foam cells) resulting in plaque disruption and atherogenic vulnerability. The cap may be compromised by the presence of inflammation and swelling. As a result, activated inflammatory cells release heat that, when detected, indicates the presence and progression of vulnerable plaque.
Many devices have been proposed to detect vulnerable plaque. Magnetic resonance imaging, nuclear imaging techniques, endovascular ultrasonography, angiography, angioscopy, infrared spectroscopy, and cardiovascular wall temperature measurements may be used to determine the presence and location of carotid, aortic and coronary atherosclerotic plaques. Included in such devices are thermal sensing catheters, as well as infrared and optical coherence tomography (OCT) catheters.
Vulnerable plaque differs from underlying tissue in that it typically has an elevated temperature. This elevated temperature, while distinct, may be difficult to detect due to the relatively small difference between the temperature of the fibrous cap and the normal vascular wall temperature. Measurement of temperature differences between vulnerable plaques and normal vessels provides direct evidence of inflammatory material in the plaque core and thin walls surrounding the core. Normal arterial wall temperatures are relatively constant, although patients with coronary artery disease of increasing severity have progressively larger temperature deviations between the plaque lesions and the baseline wall temperature. The temperature deviations range from less than 0.1 degrees centigrade for stable angina to above 1.5 degrees centigrade for acute myocardial infarction. Degradation of the cap thickness may further enhance the observable temperature differential, providing additional indications of severity and impending peril. Plaque rupture may be predicted by looking for hot spots in arterial walls that are caused by the release of heat from the activated inflammatory cells.
Invasive procedures may provide the best opportunity for vulnerable plaque identification and local treatment. Such methods are conveniently used during angioplasty or other surgical procedures when the patient is undergoing intensive procedures involving catheters.
Instrumented catheters provide imagery and sensor information as the guidewire and catheter body are manipulated through the larger arterial vessels in the body. Often catheters are inserted into the femoral artery in the thigh, and threaded up a circuitous path into the heart or through the carotid arteries and into the cerebellum. Cardiovascular wall temperatures may be extracted with thermocouple measurements from a suitably equipped guidewire. The thermocouple is tensioned with a graceful kink in the guidewire, providing direct contact with the lumen wall as the guidewire progresses through the vessels. Measurement accuracy is low due to the pulsing flow of blood in the vicinity of the thermocouple, which rapidly diffuses heat generated by the vulnerable plaque. Contact measurements present an intrinsic risk of generating fissures in the plaque wall and liberating its contents, while increasing the risk of thrombogenic responses and the potential for coronary failure.
Vulnerable plaque may be either simple, low-level lesions in an artery or may be protruding lesions in an artery. In a guidewire-based thermal sensing system, a thermal sensor is required to actually touch the vulnerable plaque lesion. When lesions protrude into the artery lumen, guidewire-based sensors may move past without touching and thus, the protruding lesions might not be detected.
Temperature measurements of the cardiovascular walls using intravascular, non-contact techniques are desirable to avoid undue traction with a vessel wall. Catheter-based apparatus may ascertain the presence and extent of vulnerable plaque, and allow for immediate, localized treatment of the atherosclerotic lesions. While non-contact, catheter-based diagnosis and treatment are attractive therapeutic methodologies for stabilization and abatement of vulnerable plaque, accurate determination of wall temperature is difficult due to the pulsating fluid flow through the vessel and around the temperature sensor. The amount of error in temperature measurement increases as a temperature sensor moves further from the vascular wall. Thermal imaging devices are similarly compromised due to varying opacities of the blood in the vessel. A measurement technique that allows accurate determination of cardiovascular wall temperature in the presence of pulsating flow within the blood vessel would be beneficial in providing an accurate assessment of the presence, severity and extent of any vulnerable plaque.
It is an object of this invention, therefore, to provide a method and system for determining vulnerable plaque and other vascular conditions using enhanced temperature-sensing techniques, to provide an option for local treatment or long term treatment of the vulnerable plaque, and to overcome the deficiencies and limitations described above.